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Lecture notes Psychopharmacology

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Lecture notes from all the lectures psychopharmacology, UU, Psychology

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  • June 14, 2023
  • 31
  • 2022/2023
  • Class notes
  • Joke baas & leon kenemans
  • All classes
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Available practice questions

Flashcards 76 Flashcards
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Some examples from this set of practice questions

1.

Agonist/antagonist: Caffeine

Answer: Antagonist

2.

Op welke neurotransmitter(s) en/of receptor werkt caffeine

Answer: Adenosine receptor

3.

Agonist/antagonist: Nicotine

Answer: Agonist

4.

Op welke neurotransmitter(s) en/of receptor werkt nicotine?

Answer: Nicotine-acetylcholine receptor (nAChR)

5.

Agonist/antagonist: Amphetamine

Answer: Antagonist

6.

Op welke neurotransmitter(s) en/of receptor werkt amphetamine

Answer: the reuptake of dopamine, noradrenaline and to a lesser extent, serotonin

7.

Agonist/antagonist: Cocaine

Answer: Antagonist

8.

Op welke neurotransmitter(s) en/of receptor werkt cocaine

Answer: Blocking noradrenaline transporters, and especially dopamine transporters

9.

Agonist/antagonist: Methylphenidate

Answer: Antagonist

10.

Op welke neurotransmitter(s) en/of receptor werkt Methylphenidate?

Answer: Blocking noradrenaline transporters, and especially dopamine transporters.

Lectures Psychopharmacology
Lecture 1
Psychopharmacology: focuses on their effects on behavior, cognition and affect (incl. their
mechanisms in the brain) -> more internal processes and behavior
Pharmacology: Studies the influence of substances on biological processes (c.q., living beings)
2/3th gets better from medication, 1/3th doesn’t benefit from it

Pharmacokinetics: ‘How does a substance move through the body?’

Pharmacodynamics: ‘What does the substance do to the body?’
 To what receptors does the substance bind?
 What effect does the substance have on the receptor
In Psychopharmacology this means: interactions with neurotransmitters

Neurotransmission
 Neurons
 Action potential
 Synapse
 Transmitter
- Synthesis
- Release
- Degradation
 Receptor




How do you get your information?
 First insight from folklore (e.g., alcohol)
 Later development often coincidence (trail and error)
 Hypothesis-based research targeted drug discovery

What is hypothesis based on?
1. Basic knowledge -> ‘preclinical research’
• How neurotransmitter levels are de- or increased
• Which brain cells/regions are involved in a brain function
• Which kinds of substances may affect a neurotransmitter
• Which kinds of substances may affect a certain type of brain cell
• What are potential beneficial and side effects of a substance
2. Clinical knowledge -> ‘Clinical research’
• Which brain functions are involved in a psychiatric disorder
• Which brain cells/regions are involved in a psychiatric disorder
• What is known about levels of neurotransmitters in a disorder
• Different subtypes if a disorder that may require different treatment

,Hypothesis-based research
1) Start with knowledge from the literature
2) What is known about a (clinical) phenomenon?
– Which neurotransmitter (NT) may affect this function?
– Which substances (medicines) may affect this NT?
– What patient characteristics may influence whether a certain approach will work (and for a given patient)?
– Is the substance prone to side effects / toxicity / addiction?
– Do the beneficial effects outweigh the side effects?
3) What is not known and would be important to find out?

When can a new substance be prescribed?
New compounds must be admitted by a regulatory board vb. FDA, CBG, EMA
- Registration for medication based on research into efficacy and safety

1) Preclinical phases (animals) on.
Efficacy (does it work? Animals might not be the same)
Administration (does the substance survive the gastro-intestinal system? And the blood-brain barrier?)
Safety: (side effects, even when administered systemically?)
Therapeutic index = relation between the toxic dose and the effective dose = TD50 / ED50
You want this to be a large number, you want the distance to big between toxic and working

TD50 / ED50: dose at which 50% shows dangerous side effects
(TD50) versus the dose at which 50% has the intended effect
(ED50)

Safety registration: Therapeutic index, drug interactions and
toxicity (expected effect, often temporary and unexpected
effects)



2) Clinical trials (in humans)
- Phase 1: Non-toxic, tolerable
Is it safe?
- Phase 2: Limited efficacy studies
Does it work?
- Phase 3: Large, multi-center studies
Does it work, and is it better than existing drugs?
- Phase 4: Monitoring after introduction
Long-term effects, optimal dose (lowest working and highest without side effects)

What’s in a name?
 Chemical name/formula
 Codename (with manufacturer)
 Generic name, easier to communicated
 Brandname when the patent expires it sold cheaper on the generic name

Drugs versus medicines: Related to their purpose: a medicine aims to cure; a drug does not
necessarily have the purpose. Hence: all medicines are drugs, whereas not all drugs are medicines.

Great disadvantage:
• Medicines must have enough market to be at least somewhat profitable

,‘Orphan drugs’/ ‘Orphan diseases’: typically, do not
- (Medicines for) relatively rare disorders
- Support from governments/ non-profit funds to fund medicines in this category
- Or: huge costs per patients

The cost of a medicine is around 802 million

Example. The timeline of Prozac (anxiety)




There is always research before and after registration

Registration
A medication can be registered for a certain indication or a certain group.
A physician is allowed to prescribe a registered medicine for another indication of group. This is called ‘off-label’ use

Tests of efficacy
- Randomized
- Placebo-controlled
Sometimes the placebo effect is as effective as the medicine
- Double blind

Evidence-based medicine (Important that its evidence-based, check reliability)
- Meta-analysis rather than relying on a single study
- Guidelines (Cochrane reviews)
- Answer to a number of clinical questions
– What is the first-choice treatment?
– How long must this be maintained?
– What to do if this treatment does not seem to work?



Lecture 2
Principles of psychopharmacology

Psychopharmacology is ‘common’ use – understand the effect on the behavior
o Improve behavior
Brain and neurotransmitters (chemical) determine behavior, manipulate via psychoactive substances
to understand behavior

Clonidine
(Zombie drug is a super clonidine with heroin (Xylazine))

,  Haloperidol works on the dopamine (D2) receptors (blocker) and clonidine works in the
norepinephrine system

Dose-response curve (DRC): The effect of certain dose what the effect is
- Effects depend on dose
- Response as function of dose
- Depends on which response you look at

Potency: The minimal dose you need for the minimum effect
Efficacy: maximum effect
Therapeutic window: How much is the side effects separated from the good effect. This is called with
the therapeutic index.

Where to start titration? -> Start with a dosage that had visible effect bit relative low side effects on
the curve. It is an average so it can be different in your subject.

Gold standard = randomized double-blind placebo-controlled trail (RCT)
Use a placebo of time of happening something else. Nobody should be informed who gets what-when
(blind). It has to be randomized so other effects are not of influence (age, sex, etc.)

DRCs for Undesired effects also show almost linear increase with increasing dose ‐e.g., dropout rate

Every (almost) have a uni linear curve, because it only goes one way to a point of saturation.
o For humans
For animals there might, but for human its not ethical. In animals it is different, because they are
different in acceptable side-effects.

Pharmacodynamics: Biochemical and psychological effects of substances

<- Dopamine receptor

The effects can be presynaptic versus postsynaptic

It can have effect on the transporter or other receptor

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